We have studied mechanisms underlying long-term potentiation (LTP) in the medial and lateral amygdala using in vitro slice preparations. In normal bathing medium, LTP was not induced by tetanic stimulation (100 pulses at 100 Hz). However, in the presence of a GABAA blocker, picrotoxin or bicuculline, LTP was reproducibly induced in both medial and lateral amygdala. In the medial amygdala, the LTP induced in the presence of picrotoxin was blocked by 2-amino-5-phosphonovalerate (APV), an NMDA receptor antagonist, and was significantly reduced by scopolamine, a muscarinic receptor antagonist. On the other hand, the LTP in the lateral amygdala was not affected by APV, but was significantly reduced by scopolamine. These results suggest that both NMDA receptors and muscarinic receptors are involved in the induction of medial amygdala LTP, while muscarinic receptors, but not NMDA receptors, are involved in the induction of lateral amygdala LTP.